Figure 9.

Possible H₂S-dependent signaling mechanisms that regulate cell death in the nervous tissue in cognitive impairment and encephalopathy. H₂S, hydrogen sulfide; CHOP, C/EBP homologous protein; Casp12, caspase-12; TRL4, toll like receptor 4; NF-ĸB, nuclear factor kappa-light-chain-enhancer of activated B cells; iNOS, inducible nitric oxide synthase; NO, nitric oxide; ROS, reactive oxygen species; PSD-9, postsynaptic density protein 95; Bax, bcl-2-like protein 4; NMDAR, N-methyl-D-aspartate receptor; IL-6, interleukin-6; IL-1β, interleukin-1β; TNF-α, tumor necrosis factor-α; Syn1, synapsin 1; LDHA, lactate dehydrogenase A; mTOR, mammalian target of rapamycin; PDK, pyruvate dehydrogenase kinase 1; SOD, superoxide dismutase; GSH, glutathione; Aco, aconitase; CS, citrate synthase; Sirt1, NAD-dependent deacetylase sirtuin-1; CK, creatine kinase; NF-ĸB p65, RelA; PD, pyruvate dehydrogenase; Bcl-2, B-cell lymphoma 2; HO-2, heme oxygenase 2; M2-PK, pyruvate kinase M2; CPR78, cuticular protein RR-2 motif 78; Nrf2, nuclear factor erythroid 2–related factor 2; ARE, antioxidant response element.